Factors which affect the diastolic pressure volume curve

Abstract

We need to reassess the direction of research on questions related to the left ventricular diastolic pressure volume relationship. To date, most workers have concentrated on developing sophisticated models of the left ventricle with the hope of computing detailed stress distributions or inferring changes in muscle elasticity with disease, especially coronary artery disease. Unfortunately, one cannot obtain enough information from the short segment of the diastolic pressure-volume curve available clinically to compute any of the proposed ventricular stiffness parameters. The fact that the relationship between end-diastolic volume and pressure changes on a beat-to-beat basis undermines traditional ventricular function curves, since such changes in diastolic pressure-volume curve shift the ventricular function curve just as do changes in systolic peformance. The theoretical, experimental, and clinical results we have reviewed suggest that geometry changes, i.e. hypertrophy and dilation, influence the pressure-volume curve in response to chronic changes in the heart's operating environment. Acute reversible muscle elasticity changes are much smaller than have been expected and are probably inadequate to explain acute shifts in the pressure-volume curve. In addition, direct experimental studies on dog hearts with the effects of the right ventricle minimized failed to detect changes in the pressure-volume curve with either segmental or global ischemia. Changes in muscle elasticity, however, play an important role in mediating some chronic shifts in the pressure-volume curve, such as those which develop following the development of fibrosis. Whether or not viscoelastic effects are physiologically significant remains to be resolved. Incomplete relaxation and coronary circulation engorgement are probably not significant determinants of the pressure-volume curve or mechanisms which produce the shifts that have been observed in both acute and chronic situations. Strong evidence supports a role for the interaction between the right and left ventricles in regulating the left ventricular diastolic pressure-volume relationship. Future work should seek to understand better the variation in the pressure-volume curve and its relationship to systolic function, as well as to determine whether or not manipulating this variation can be used as a therapeutic intervention to treat left heart disease.